Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

506 patients with schizophrenia, diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-III) criteria, were included in a long term treatment programme with remoxipride, a selective dopamine (D2)-receptor antagonist. This overview includes pooled data from all patients who have been treated long term with remoxipride in clinical trials, focusing on patients treated for more than 6 months (n = 283). Remoxipride was administered in daily doses of 75 to 600mg. The assessment tools were Brief Psychiatric Rating Scale (BPRS), Clinical Global Impression (CGI), Simpson and Angus scale, Abnormal Involuntary Movements Scale (AIMS) for abnormal involuntary movements, adverse events/symptoms using a 26-item checklist, clinical chemistry, and haematology and cardiovascular investigations. The majority of patients had a long duration of illness (median 11 years). 67% of patients (340/506) withdrew from treatment before 12 months and 44% (223/506) stopped treatment before 6 months. The median BPRS total score decreased during the first 3 months from 23 to 12, and this level of improvement was maintained throughout the 12-month period. Treatment-emergent adverse events reported by more than 5% of the patients were insomnia, tiredness, drowsiness and tremor in the group treated for 6 to 12 months. No symptoms, including checklist extrapyramidal symptoms (EPS), were reported by more than 5% of patients treated for 12 months. Low frequencies of EPS according to the Simpson and Angus scale were seen in patients treated for more than 6 months (n = 147). A small but statistically significant reduction of the mean total AIMS score from baseline to last rating was observed. There were infrequent changes in heart rate, resting diastolic blood pressure and electrocardiogram (ECG). Clinical chemistry and haematology data showed no evidence of clinically significant changes over time during the 12 months of treatment. Among 506 patients, 7 suicides and 7 suicide attempts occurred during the study period. Other serious adverse events were abnormal liver function test (2 cases), gastrointestinal, urinary retention, status epilepticus (psychotic polydipsia), granulocytopenia (1 each) and myocardial infarction (5 cases). Remoxipride is of potential value as a drug which is both effective and well tolerated in the long term management of patients with schizophrenia.
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PMID:Tolerability of remoxipride in the long term treatment of schizophrenia. An overview. 832 49

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59

Hereditary chin trembling is a rare autosomal dominant disease often considered as an "essential tremor variant". The clinical and neurophysiological data obtained in a new white family lead to the suggestion that this abnormal involuntary movement is a focal variant of hereditary essential myoclonus.
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PMID:Hereditary chin trembling or hereditary chin myoclonus? 941 23

Stimulation of the thalamic nucleus ventralis intermedius (Vim) at high (130-Hz) frequency has been used over the last 8 years as a treatment in 134 patients with movement disorders (91 Parkinson's disease [PD], 23 essential tremor [ET], 21 various dyskinesias and dystonias, including four multiple sclerosis [MS]), implanted with long-term electrodes connected to a programmable stimulator. In PD patients, tremor was selectively suppressed for < or = 11 years. In ET patients, results were satisfactory, but in 35% of the cases deteriorated with time, when tremor had an action component. Other types of dyskinesias were much less influenced. Sixty-eight patients were bilaterally implanted, and 14 were implanted contralateral to a previous thalamotomy. Side effects were often minor, well tolerated, and immediately reversible. Three secondary scalp infections led to temporary removal of implanted material. There was no permanent morbidity. Long-term Vim stimulation, which is reversible, adaptable, and well tolerated, even by bilaterally operated-on (68 of 134) and by elderly patients, should replace thalamotomy in the regular surgical treatment of parkinsonian and essential tremors. More recently, we stimulated the subthalamic nucleus (STN) in 51 patients (44 bilateral) and the globus pallidus internus (GPi) in 12 patients (seven bilateral). STN stimulation has a spectacular effect on akinesia and rigidity and may improve the patients so as to maintain them all day at a level similar to their best "on" periods. A 30-50% reduction in drug dosage was possible in most of the patients. GPi stimulation has indications and effects similar to those of pallidectomy: abnormal involuntary movements are totally suppressed, whereas effects on akinesia and rigidity are not so important as they are with STN stimulation. For all three targets, morbidity is low and reversible, even when bilateral implantations are performed. The deep-brain stimulation method has now proved its safety as compared with ablative surgery and is able to provide a significant improvement to these severely disabled patients. Long-term follow up is establishing the security of the method, which should be considered in earlier stages of the disease actively to participate to rehabilitation.
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PMID:Long-term electrical inhibition of deep brain targets in movement disorders. 982 7

We report a 73-year-old Japanese woman with familial Parkinson's disease. The patient was well until her 67 years of the age, when she noted rest tremor in her right hand. Soon after her gait became short stepped. She visited our clinic on October 6, 1992 when she was 68 years old. She was alert and well oriented without dementia. She showed masked face, small voice, small stepped gait, retropulsion, resting tremor in her right hand, rigidity in the neck, and bradykinesia. She was treated with 400 mg/day of levodopa-carbidopa, which improved her symptoms, however, she developed wearing off phenomenon 3 years after the initiation of levodopa treatment. On August 26, 1998, she developed abdominal pain, diarrhea, and vomiting. She was admitted to another hospital, where abdominal plain x-ray revealed an evidence of intestinal obstruction (ileus). She was treated with nasogastric suction and intravenous fluid. Her condition did not improve and she was transferred to our hospital on August 29, 1998. Her family history revealed no consanguineous marriage. She had two elder brothers and three elder sisters. One of her brothers had been diagnosed as Parkinson's disease. Her husband also suffered from Parkinson's disease, however, her parents apparently did not have Parkinson's disease. On admission, she appeared to be drowsy. Her blood pressure was 102/70 mmHg, body temperature 36.2 degrees C. The lungs were clear and no cardiac murmur was present. Abdomen was flat and bowel sound was audible. No abnormal mass was palpable. Neurologic examination revealed mild consciousness disturbance, masked face, and small voice. No motor paralysis was noted. Muscle tone was hypotonic. No abnormal involuntary movement was noted. Abnormal laboratory findings on admission were as follows; WBC 11,300/microliter, amylase 1,373 IU/l, CK 446 IU/l, BUN 50 mg/dl, creatinine 1.17 mg/dl, CRP 22.7 mg/ dl, Na 134 mEq/l, K 3.1 mEq/l, and Cl 81 mEq/l. A chest x-ray film revealed pneumonic shadows in both lower lung fields. She was treated by nasointestinal suction, intravenous fluids, and chemotherapy for her infection. Her BP started to drop on September 2 and she developed cardiac arrest on the same day. She was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had a form of autosomal dominant familial Parkinson's disease. As parents did not have Parkinson's disease, some of the participants raised the possibility of autosomal recessive inheritance. But the age of onset was too late for autosomal recessive inheritance. Majority thought that the mode of inheritance was autosomal dominant with low penetrance. alpha-Synuclein mutation causes an autosomal dominant familial Parkinson's disease, but this type is very rare in non-Greek populations and the penetrance is high. Chromosome 2-linked autosomal dominant familial Parkinson's disease shows low penetrance. There are many other autosomal dominant forms of familial Parkinson's disease linked to yet unknown chromosome loci. Majority thought that this patient also had a form of Lewy-body positive autosomal dominant familial Parkinson's disease of unknown chromosome locus. Post mortem examination revealed ischemic intestinal lesion with strangulation. This was thought to be the cause of her death. In the central nervous system, the brain appeared to be normal by inspection. In the coronal sections, the substantia nigra and the locus coeruleus showed marked depigmentation. Histologic examination revealed marked neuronal loss and Lewy body formation in the remaining neurons. Pathologic examination was consistent with Parkinson's disease. Mutational analysis for the parkin gene was negative.
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PMID:[A 73-year-old woman with familial Parkinson's disease]. 1065 9

A case of acute encephalopathy with selective bilateral symmetrical striatal lesions is reported. The patient was a previously healthy 4-year-old boy who became obtunded after a febrile illness and fell into a state of delirium with severe pain in the feet. He showed abnormal postures: hyperextension of the neck and upper limbs and extreme flexion of both lower limbs, and abnormal involuntary movements of the limbs: tremor, athetotic movement and right hemiballismus. Analysis of serum antibody titres suggested recent primary infection of herpes simplex type 1 (HSV-1). Cranial T2-weighted magnetic resonance imaging (MRI) demonstrated areas of high-signal intensity involving the whole basal ganglia bilaterally. He showed rapid clinical improvement after the initiation of corticosteroid therapy; complete clinical recovery was noted 3 months after the onset. Serial MRI studies demonstrated a rapid reduction of the lesions, resulting in only slight T2-hyperintense areas in both caudate nuclei. The pathogenesis of the disorder remains unknown, though an autoimmune mechanism has been speculated. The clinical and laboratory findings in this case suggested a possible role of HSV-1 in the pathomechanism of the disorder and a beneficial effect of early corticosteroid therapy.
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PMID:Acute encephalopathy with bilateral striatal necrosis: favourable response to corticosteroid therapy. 1072 92

GAIT ARRESTS: They affect the evolution of the disease. This freezing phenomenon which induces falls sometimes constitutes an initial sign. Like the gait initiation failure, freezing can be controlled by sensory stimulation, notably visual inputs, but also by more sustained attention. FALLS ARE MAINLY CONNECTED WITH BOTH POSTURAL INSTABILITY AND RIGIDITY: They are poorly influenced by dopaminergic therapies. The progressive decrease of step width represents a main factor in their occurrence. PRECOCITY OF GAIT DISORDERS IS UNUSUAL IN PARKINSON'S DISEASE: Other parkinsonian syndromes such as progressive supranuclear palsy, multiple system atrophy and vascular parkinsonian syndrome must then be evoked. Their association with a cognitive impairment and abnormal sphincter behaviour infers a diagnosis of normal pressure hydrocephalus. GAIT IMPROVES WITH L-DOPA THERAPY: Speed, step length and duration of the swing phase are increased without change of cadence. Progressive loss of L-dopa efficiency on gait and postural stability contrasts with the persistent effect on tremor, rigidity and bradykinesia; a functional abnormality of nondopaminergic systems can explain these symptoms. In the following stages, gait troubles increased by motor fluctuations and abnormal involuntary movements are less controlled by L-dopa therapy. PHYSICAL THERAPY PLAYS A MAJOR ROLE IN THERAPEUTIC MANAGEMENT: An individual or collective rehabilitation project must be established according to the stage of evolution; the exercises aim to protect postural control and coordination. Visual or sound rhythmic inputs can be employed in the case of gait initiation failure. THE EFFECTS OF FUNCTIONAL NEUROSURGERY ARE IN THE COURSE OF EVALUATION: Thermolesion and chronic electrical stimulation of deep brain structures have opposite effects on gait troubles. Bilateral thalamotomy or pallidotomy are sometimes a source of disequilibrium. Chronic thalamic stimulation does not induce either benefits or adverse effects. On the other hand, stimulation of the internal pallidum improves gait kinematic parameters; improved postural adjustments have also been reported. The effect of subthalamic nucleus stimulation is comparable to that of L-dopa, however the long-term effect remains to be evaluated.
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PMID:[Gait disorders in Parkinson disease. Gait freezing and falls: therapeutic management]. 1128 86

Abnormal involuntary movements are common symptoms in children. The neuroanatomical basis for these movement disorders is the extrapyramidal system. Although present at rest they may be more intensive during the will - depending motor activity and increased under stress. They are almost absent during sleep. The underlying causal factors of involuntary movement disorders include metabolic disorders, progressive neurodegenarative diseases, central nervous system infection. The symptomatology of chorea, athetosis, dystonia, tremor, myoclonus and tics are discussed. Special attention is paid to differential diagnosis of myoclonus, chorea and tics as well as to movement disorders and epilepsy.
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PMID:[Symptomatology of movement disorders in children]. 1167 82

We report on the case of a patient with transient tongue tremor and coma after electrical injury, probably due to a reversible brainstem dysfunction. We then reviewed the differential diagnosis of abnormal involuntary movements of the tongue as well as movement disorders related to electrocution.
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PMID:Tongue tremor in a patient with coma after electrical injury. 1281 67

Jaw tremor can be seen as a component of various neurological disorders such as essential tremor, Parkinson's disease, dystonia, branchial myoclonus, hereditary geniospasm, task-specific tremor, and Whipple's disease, as well as in normal situations such as shivering, and subclinical physiological jaw tremor. In most of these conditions, the jaw tremor is usually associated with tremor or other abnormal involuntary movements affecting additional body parts, and its frequency is lower than 12 Hz. Schrag and colleagues reported a patient with a high-frequency idiopathic jaw tremor, and they speculated it could be related to orthostatic tremor affecting the masseter muscles. We encountered a similar patient with intermittent rapid focal jaw tremor that was successfully treated with botulinum toxin injections to the masseters.
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PMID:Isolated high-frequency jaw tremor relieved by botulinum toxin injections. 1660 5


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